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Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
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Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
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Related Experiment Video

Updated: Sep 6, 2025

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy
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Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy

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Glycan degradation promotes macroautophagy.

Alice D Baudot1, Victoria M-Y Wang1, Josh D Leach1,2

  • 1Tumour Cell Death and Autophagy Laboratory, Cancer Research UK Beatson Institute, Glasgow G61 1BD, United Kingdom.

Proceedings of the National Academy of Sciences of the United States of America
|June 23, 2022
PubMed
Summary

Macroautophagy relies on glycan degradation by α-l-fucosidase 1 (FUCA1). Impaired FUCA1 function leads to defective autophagy and contributes to fucosidosis disease progression.

Keywords:
fucosidosislysosomesmacroautophagyα-l-fucosidase 1

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Lysosomal Biology

Background:

  • Macroautophagy maintains cellular homeostasis by degrading cytoplasmic components via lysosomes.
  • While protein degradation is well-studied, the role of glycan degradation in autophagy remains less understood.

Purpose of the Study:

  • To investigate the role of glycan degradation in macroautophagy.
  • To explore the function of α-l-fucosidase 1 (FUCA1) in autophagic flux and its implications in fucosidosis.

Main Methods:

  • Utilized FUCA1-null cells and a mouse model of fucosidosis.
  • Employed lectin capture and mass spectrometry to analyze lysosomal enzyme fucosylation.
  • Assessed autophagic flux and autophagosome-lysosome fusion.

Main Results:

  • Cells lacking FUCA1 accumulate lysosomal glycans, leading to impaired autophagic flux.
  • In fucosidosis models, glycan accumulation and autophagosome buildup correlate with tissue damage.
  • FUCA1 deficiency alters lysosomal enzyme fucosylation, hindering enzyme activity induction and autophagosome-lysosome fusion.

Conclusions:

  • Glycan degradation by FUCA1 is essential for proper macroautophagy.
  • Dysregulated glycan metabolism contributes to defective autophagy, a likely factor in fucosidosis pathogenesis.